Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA133267 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE23169: Transcriptional profiling of Ramos germinal center B cells GSE23170: ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells Refer to individual Series
2012-01-01 | E-GEOD-23171 | biostudies-arrayexpress
Project description:ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells. The goal was to combine information from our ChIP-on-chip and expression array analyses to compile a list of CRTC2 target genes.
2012-01-01 | GSE23170 | GEO
Project description:ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells. The goal was to combine information from our ChIP-on-chip and expression array analyses to compile a list of CRTC2 target genes. CRTC2 was immunoprecipitated from sheared chromatin isolated from untreated Ramos cells using 2 antibodies which recognize distinct epitopes on the CRTC2 protein. Immunoprecipitates were compared to total input chromatin. 2 biological replicates were performed for each antibody.
2012-01-01 | E-GEOD-23170 | biostudies-arrayexpress
Project description:Transcriptional profiling of Ramos germinal center B cells, comparing untreated cells to cells treated with etoposide, and untreated cells to cells treated with anti-IgM. Both treatments, engagement of the B-cell receptor with anti-IgM and induction of DNA double-strand breaks with etoposide, result in phosphorylation and cytoplasmic sequestration of CRTC2, and cause downregulation of known CRTC2 target gene TCL1. The goal of these experiments was to determine what other genes are downregulated by both of these CRTC2-inactivating treatments, and to compare this list to the list of genes whose promoters were occupied by CRTC2 in our ChIP-on-chip assay. Untreated samples vs. etoposide-treated samples, untreated samples vs. anti-IgM-treated samples. Each comparison was done in biological triplicate plus dye swap.
2012-01-01 | E-GEOD-23169 | biostudies-arrayexpress
Project description:Transcriptional profiling of Ramos germinal center B cells, comparing untreated cells to cells treated with etoposide, and untreated cells to cells treated with anti-IgM. Both treatments, engagement of the B-cell receptor with anti-IgM and induction of DNA double-strand breaks with etoposide, result in phosphorylation and cytoplasmic sequestration of CRTC2, and cause downregulation of known CRTC2 target gene TCL1. The goal of these experiments was to determine what other genes are downregulated by both of these CRTC2-inactivating treatments, and to compare this list to the list of genes whose promoters were occupied by CRTC2 in our ChIP-on-chip assay.
2012-01-01 | GSE23169 | GEO
Project description:Transcriptional profiling of Ramos germinal center B cells
| PRJNA133273 | ENA
Project description:Germinal center B cells were isolated from human tonsil tissue and crosslinked. ChIP was performed on two distinct pools of germinal center cells, each obtained from 3-5 donors. The experiment includes two biological replicates (germinal center cell pools from different donors). ChIP was performed on both pools and subject to library preparation and sequencing. Input DNA was sequenced for both pools.
2015-12-04 | E-GEOD-68349 | biostudies-arrayexpress
Project description:The antibody gene mutator AID promiscuously damages oncogenes and B cell identity genes leading to chromosomal translocations and tumorigenesis. Why non-immunoglobulin loci are susceptible to AID activity is unknown. Here we study AID-mediated lesions in the context of nuclear architecture and the B cell regulome. We show that AID targets are not randomly distributed across the genome, but are predominantly clustered within super-enhancers. Unexpectedly, in these domains AID deaminates highly active promoters and eRNA+ enhancers interconnected in some instances over megabases of linear chromatin. Using genome editing we demonstrate that 3D-linked targets cooperate to recruit AID-mediated breaks. Furthermore, a comparison of hypermutation in mouse B cells, AID-induced kataegis in human lymphomas, and translocations in MEFs reveals that AID damages different genes in different cell types. Yet, in all cases, the targets are predominantly associated with topological complex, highly transcribed super-enhancers, demonstrating that these compartments are key mediators of AID recruitment. Examination of AID activity in human cells via Single Nucleotide Variant discovery in H3K4me3 ChIP-seq data from 26 MSH2-/-; AIDtg; UGItg, 18 AICDA-/- and 2 unmodified RAMOS clonal populations. Examination of PolII mediated long-range interactions via Chia-PET of RAMOS cells (2 sample). Identification of super-enhancers from H3K27Ac ChIP-Seq data from activated B cells (3 replicates and 1 input control) and RAMOS cells (1 sample and 1 input control), 2 preparations of naive and 2 of germinal center (GC) B cells from human tonsilectomy samples. Mapping of regulatory elements in RAMOS based on H3K4me1 (1 sample) and Nipbl (2 replicates) ChIP-Seq. RNA expression analyses of activated B cells from 3 WT and 3 Il4raU/U mice and RAMOS cells (3 replicates). Mapping of long-range interactions by 4C in activated B cells from a WT and an Il4raU/U mouse with the IL4ra and Il21r locus, respectively, as a viewpoint. Mapping of Super-Enhancers in activated B cells from Il4raU/U and WT control mice (2 samples).
2014-12-04 | E-GEOD-62063 | biostudies-arrayexpress
Project description:Follicular lymphomas and diffuse large B-cell lymphomas have markedly different biological phenotypes and yet all originate from mature, germinal center B-cells. We hypothesized that alterations in DNA methylation patterning might help explain the clinical heterogeneity of these diseases. We report that intra- and inter-individual patient heterogeneity in cytosine methylation is associated with disease severity, and that methylation heterogeneity originates in germinal centers and is amplified during disease progression. Abnormal methylation patterns differ between chromosomal regions and depend on local gene density and the methylation status of neighboring genes. Lymphomagenic transcriptional regulators, such as BCL6, MYC and EZH2, perturb DNA methylation in a target gene-specific manner. Furthermore, aberrant epigenetic states – especially hypomethylation – tend to spread along DNA in a non-specific manner while insulator elements like CTCF inhibit such spreading. Our findings suggest mechanisms through which altered cytosine methylation contributes to the distinct phenotypes of tumors derived from mature B-cells. Identification of MYC target genes in Burkitt lymphomas by ChIP-on-chip. MYC ChIP-on-chip was done in two Burkitt Lymphoma (BL) cell lines (ramos and mutu3) in duplicate. This submission represents the ChIP-chip component of the study.
2012-11-27 | E-GEOD-31110 | biostudies-arrayexpress
Project description:Germinal center B cells were isolated from human tonsil tissue and crosslinked. ChIP was performed on two distinct pools of germinal center cells, each obtained from 3-5 donors.
2015-12-04 | GSE68349 | GEO